Blood-nerve barrier Permeability to ions and nonelectrolytes is very low, indicating limited exchange between plasma and nerve endoneurium. The nerve barrier, unlike the brain barrier, appears not to have a regulatory transport system for calcium. As a result, nerve calcium concentration varies with the plasma calcium concentration. Glucose and amino acids are taken up into nerve from plasma by facilitated transport systems located at the endoneurial endothelium. The transport systems accelerate nerve uptake of nutrients, and allow matching of transport to metabolic demand. Permeabilities of both nerve capillaries and perineurium increase during the first few weeks following nerve damage and Wallerian degeneration. Nerve capillary permeability eventually returns to normal, b%At perineurial permeability remains elevated, suggesting that nerve fibers are required to maintain perineurial nerve barrier integrity. Blood-nerve barrier permeability and nerve water content were found to increase in rats fed high -galactose diets-for 11 months. Both changes could be prevented by treatment with aldose reductase inhibitors, such as Statil and Alconil, consistent with the "polyol" hypothesis of galactose neuropathy.